scholarly journals Biochemical Signals Mediate the Crosstalk between Cartilage and Bone in Osteoarthritis

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Xuchang Zhou ◽  
Hong Cao ◽  
Yu Yuan ◽  
Wei Wu

Osteochondral junction is a functional unit comprising the articular cartilage, calcified cartilage, and subchondral bone. Alteration in any component of this composite unit can disrupt the joint integrity and function directly or indirectly. Biochemical signals mediate the crosstalk between tissues and play an essential role in the initiation and progression of osteoarthritis. As osteoarthritis progresses, abnormal subchondral bone remodelling leads to increased angiogenesis and porosity of the subchondral bone plate, which further triggers biochemical signals to mediate the crosstalk between cartilage and bone, contributing to the progression of osteoarthritis. Notably, common biochemical signals include the TGF-β/Smad, Wnt/β-catenin, RANK/RANKL/OPG, and MAPK pathways. This biomarker crosstalk network is the basis of osteoarthritis pathogenesis, and some of their key regulators may be potential therapeutic targets for osteoarthritis drug therapy. This review summarised the biochemical crosstalk between cartilage and bone in the pathogenesis of osteoarthritis, which may provide the basis for the discovery of osteoarthritis treatment targets.

2019 ◽  
Vol 27 ◽  
pp. S160-S161
Author(s):  
S. Das Gupta ◽  
M.A. Finnilä ◽  
S.S. Karhula ◽  
R. Korhonen ◽  
A. Thambyah ◽  
...  

2017 ◽  
Vol 06 (04) ◽  
pp. 307-315 ◽  
Author(s):  
Gregory Bain ◽  
Tom McNaughton ◽  
Ruth Williams ◽  
Simon MacLean

Background There is a paucity of information on the microstructure of the distal radius, and how this relates to its morphology and function. Purpose This study aims to assess the microanatomical structure of the distal radius, and relate this to its morphology, function, and modes of failure. Methods Six dry adult skeletal distal radii were examined with microcomputed tomography scan and analyzed with specialist computer software. From 3D and 2D images, the subchondral, cortical, and medullary trabecular were assessed and interpreted based on the overall morphology of the radius. Results The expanded distal radial metaphysis provides a wide articular surface for distributing the articular load. The extrinsic wrist ligaments are positioned around the articular perimeter, except on the dorsal radial corner. The subchondral bone plate is a 2 mm multilaminar lattice structure, which is thicker below the areas of the maximal articular load. There are spherical voids distally, which become ovoid proximally, which assist in absorbing articular impact. It does not have Haversian canals. From the volar aspect of the lunate facet, there are thick trabecular columns that insert into the volar cortex of the radius at the metaphyseal–diaphyseal junction. For the remainder of the subchondral bone plate, there is an intermediate trabecular network, which transmits the load to the intermediate trabeculae and then to the trabecular arches. The arches pass proximally and coalesce with the ridges of the diaphyseal cortex. Conclusion The distal radius morphology is similar to an arch bridge. The subchondral bone plate resembles the smooth deck of the bridge that interacts with the mobile load. The load is transmitted to the rim, intermediate struts, and arches. The metaphyseal arches allow the joint loading forces to be transmitted proximally and laterally, providing compression at all levels and avoiding tension. The arches have a natural ability to absorb the impact which protects the articular surface. The distal radius absorbs and transmits the articular impact to the medullary cortex and intermediate trabeculae. The medullary arches are positioned to transmit the load from the intermediate trabeculae to the diaphysis. Clinical Relevance The microstructure of the distal radius is likely to be important for physiological loading of the radius. The subchondral bone plate is a unique structure that is different to the cancellous and cortical bone. All three bone types have different functions. The unique morphology and microstructure of the distal radius allow it to transmit load and protect the articular cartilage.


2012 ◽  
Vol 4 (4) ◽  
pp. 249-258 ◽  
Author(s):  
Steven R. Goldring

The articular cartilage and the subchondral bone form a biocomposite that is uniquely adapted to the transfer of loads across the diarthrodial joint. During the evolution of the osteoarthritic process biomechanical and biological processes result in alterations in the composition, structure and functional properties of these tissues. Given the intimate contact between the cartilage and bone, alterations of either tissue will modulate the properties and function of the other joint component. The changes in periarticular bone tend to occur very early in the development of OA. Although chondrocytes also have the capacity to modulate their functional state in response to loading, the capacity of these cells to repair and modify their surrounding extracellular matrix is relatively limited in comparison to the adjacent subchondral bone. This differential adaptive capacity likely underlies the more rapid appearance of detectable skeletal changes in OA in comparison to the articular cartilage. The OA changes in periarticular bone include increases in subchondral cortical bone thickness, gradual decreases in subchondral trabeular bone mass, formation of marginal joint osteophytes, development of bone cysts and advancement of the zone of calcified cartilage between the articular cartilage and subchondral bone. The expansion of the zone of calcified cartilage contributes to overall thinning of the articular cartilage. The mechanisms involved in this process include the release of soluble mediators from chondrocytes in the deep zones of the articular cartilage and/or the influences of microcracks that have initiated focal remodeling in the calcified cartilage and subchondral bone in an attempt to repair the microdamage. There is the need for further studies to define the pathophysiological mechanisms involved in the interaction between subchondral bone and articular cartilage and for applying this information to the development of therapeutic interventions to improve the outcomes in patients with OA.


2016 ◽  
Vol 75 (Suppl 2) ◽  
pp. 184.1-184
Author(s):  
A.W. Nielsen ◽  
L.B. Hartlev ◽  
R. Klose-Jensen ◽  
L.W. Boel ◽  
K.K. Keller ◽  
...  

2006 ◽  
Vol 19 (03) ◽  
pp. 142-146 ◽  
Author(s):  
D. D. Frisbie ◽  
M. W. Cross ◽  
C. W. McIlwraith

SummaryHistological measurements of the thickness of non-calcified and calcified cartilage, as well as the subchondral bone plate in five locations on the femoral trochlea and medial femoral condyles of species were used in preclinical studies of articular cartilage and compared to those of the human knee. Cadaver specimens were obtained of six human knees, as well as six equine, six goat, six dog, six sheep and six rabbit stifle joints (the animal equivalent of the human knee). Specimens were taken from the lateral trochlear ridge, medial trochlear ridge and medial femoral condyle. After histopathological processing, the thickness of non-calcified and calcified cartilage layers, as well as the subchondral bone plate, was measured. Average articular cartilage thickness over five locations were 2.2–2.5 mm for human, 0.3 mm for rabbit, 0.4–0.5 mm for sheep, 0.6–1.3 mm for dog, 0.7–1.5 mm for goat and 1.5–2 mm for horse. The horse provides the closest approximation to humans in terms of articular cartilage thickness, and this approximation is considered relevant in pre-clinical studies of cartilage healing.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Zaitunnatakhin Zamli ◽  
Kate Robson Brown ◽  
John F. Tarlton ◽  
Mike A. Adams ◽  
Georgina E. Torlot ◽  
...  

Osteoarthritis (OA) is the most common joint disorder characterised by bone remodelling and cartilage degradation and associated with chondrocyte apoptosis. These processes were investigated at 10, 16, 24, and 30 weeks in Dunkin Hartley (DH) and Bristol Strain 2 (BS2) guinea pigs that develop OA spontaneously. Both strains had a more pronounced chondrocyte apoptosis, cartilage degradation, and subchondral bone changes in the medial than the lateral side of the tibia, and between strains, the changes were always greater and faster in DH than BS2. In the medial side, a significant increase of chondrocyte apoptosis and cartilage degradation was observed in DH between 24 and 30 weeks of age preceded by a progressive thickening and stiffening of subchondral bone plate (Sbp). The Sbp thickness consistently increased over the 30-week study period but the bone mineral density (BMD) of the Sbp gradually decreased after 16 weeks. The absence of these changes in the medial side of BS2 may indicate that the Sbp of DH was undergoing remodelling. Chondrocyte apoptosis was largely confined to the deep zone of articular cartilage and correlated with thickness of the subchondral bone plate suggesting that cartilage degradation and chondrocyte apoptosis may be a consequence of continuous bone remodelling during the development of OA in these animal models of OA.


1999 ◽  
Vol 195 (1) ◽  
pp. 101-110
Author(s):  
BAOHUA LI ◽  
DEBORAH MARSHALL ◽  
MARTIN ROE ◽  
RICHARD M. ASPDEN

The subchondral bone plate supports the articular cartilage in diarthrodial joints. It has a significant mechanical function in transmitting loads from the cartilage into the underlying cancellous bone and has been implicated in the destruction of cartilage in osteoarthritis (OA) and its sparing in osteoporosis (OP), but little is known of its composition, structure or material properties. This study investigated the microscopic appearance and mineral composition of the subchondral bone plate in femoral heads from patients with OA or OP to determine how these correspond to changes in composition and stiffness found in other studies. Freeze-fractured full-depth samples of the subchondral bone plate from the femoral heads of patients with osteoarthritis, osteoporosis or a matched control group were examined using back scattered and secondary emission scanning electron microscopy. Other samples were embedded and polished and examined using back-scattered electron microscopy and electron probe microanalysis. The appearances of the samples from the normal and osteoporotic patients were very similar, with the subchondral bone plate overlayed by a layer of calcified cartilage. Osteoporotic samples presented a more uniform fracture surface and the relative thicknesses of the layers appeared to be different. In contrast, the OA bone plate appeared to be porous and have a much more textured surface. There were occasional sites of microtrabecular bone formation between the trabeculae of the underlying cancellous bone, which were not seen in the other groups, and more numerous osteoclast resorption pits. The calcified cartilage layer was almost absent and the bone plate was apparently thickened. The appearance of the osteoarthritic subchondral bone plate was, therefore, considerably different from both the normal and the osteoporotic, strongly indicative of abnormal cellular activity.


2014 ◽  
Vol 155 (26) ◽  
pp. 1011-1018 ◽  
Author(s):  
György Végvári ◽  
Edina Vidéki

Plants seem to be rather defenceless, they are unable to do motion, have no nervous system or immune system unlike animals. Besides this, plants do have hormones, though these substances are produced not in glands. In view of their complexity they lagged behind animals, however, plant organisms show large scale integration in their structure and function. In higher plants, such as in animals, the intercellular communication is fulfilled through chemical messengers. These specific compounds in plants are called phytohormones, or in a wide sense, bioregulators. Even a small quantity of these endogenous organic compounds are able to regulate the operation, growth and development of higher plants, and keep the connection between cells, tissues and synergy beween organs. Since they do not have nervous and immume systems, phytohormones play essential role in plants’ life. Orv. Hetil., 2014, 155(26), 1011–1018.


Sign in / Sign up

Export Citation Format

Share Document